United States Pollution Prevention February 1995
Environmental Protection and Toxics EPA 749-F-95-015a
Agency (7407)
OPPT Chemical Fact Sheets
Nitrobenzene Fact Sheet: Support Document (CAS No. 98-95-3)
This summary is based on information retrieved from a systematic search
limited to secondary sources (see Appendix A). These sources include
online databases, unpublished EPA information, government publications,
review documents, and standard reference materials. The literature search
was done in February of 1995. No attempt has been made to verify
information from these databases or secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical/chemical properties of nitrobenzene
are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF
NITROBENZENE
____________________________________________________________________________________________
Characteristic/Property Data Reference
____________________________________________________________________________________________
CAS No. 98-95-3
Common Synonyms nitrobenzol; oil of mirbane U.S. EPA 1994
Molecular Formula C6H5NO2
Chemical Structure
Physical State liquid U.S. EPA 1985
Molecular Weight 123.06 U.S. EPA 1985
Melting Point 5.85øC @ 760 Torr U.S. EPA 1985
Boiling Point 210.9øC @ 1 atm U.S. EPA 1985
Water Solubility 1.9 g/L @ 20øC; 2.1 g/L @ 25øC U.S. EPA 1985
Specific Gravity 1.199 @ 24/4øC U.S. EPA 1985
Vapor Density (air = 1) 4.1 U.S. EPA 1985
KOC 36-650 (estimated) U.S. EPA 1987
Log KOW 1.85 U.S. EPA 1987
Vapor Pressure 0.15 mm Hg @ 20øC; 0.27 mm Hg @ 25øC U.S. EPA 1987
Reactivity flammable
Flash Point 88øC (closed cup) Budavari 1989
Henry's Law Constant 2.3 x 10-5 atm-m3/mole @ 25øC U.S. EPA 1985
Fish Bioconcentration Factor <10-15 (measured in
the golden orfe) U.S. EPA 1985
Odor Threshold perception, 0.0182 mg/m3 (3.6 ppb) Verschueren 1983
threshold, 1.9 ppm U.S. EPA 1985
Conversion Factors (in air) 1 ppm = 5.12 mg/m3;
1 mg/m3 = 0.20 ppm Verschueren 1983
___________________________________________________________________________________________
II. PRODUCTION, USE, AND TRENDS
A. Production
There were four producers of nitrobenzene in the United States in
1991: First Chemicals Corp, Mobay, DuPont Chemicals, and Rubicon,
Inc. In 1991, the estimated total production capacity of nitrobenzene
in the U.S. was 1,360 million pounds (Mannsville 1991).
Table 2 shows the producers, plant locations, and 1991 plant
production capacities of
nitrobenzene.
TABLE 2. U. S. PRODUCERS OF NITROBENZENE AND THEIR PRODUCTION
CAPACITIES
___________________________________________________________________________
Producer Location 1991 Capacity
(Millions of Pounds)
___________________________________________________________________________
DuPont Beaumont, TX 375
First Chemical Corp. Pascagoula, MS 425
Mobay (now Bayer) New Martinsville, WV 60
Rubicon, Inc. Geismar, LA 500
TOTAL 1,360
___________________________________________________________________________
Source: Mannsville 1991.
B. Uses
While nitrobenzene is primarily used in the production of aniline and
aniline derivatives, such as methyl diphenyl diisocyanate (MDI), it
also finds use in the manufacture of rubber chemicals, pesticides,
dyes, and pharmaceuticals. Nitrobenzene is also used in shoe and
floor polishes, leather dressings, paint solvents, and other materials
to mask unpleasant odors. Substitution reactions with nitrobenzene
are used to form m-derivatives (Mannsville 1991; Sittig 1991). Redis-
tilled, as oil of mirbane, nitrobenzene has been used as an
inexpensive perfume for soaps. A significant merchant market for
nitrobenzene is its use in the production of the analgesic acetamino-
phen (Mannsville 1991). Table 3 presents the estimated 1991 U. S.
end-use pattern for nitrobenzene.
TABLE 3. END-USE PATTERN OF NITROBENZENE--1991 ESTIMATE
_______________________________________________________________
Derivative Percent
(Typical Standard Industrial
Classification (SIC) Code)
Aniline
(production, SIC 2865) 97
Other 3
_______________________________________________________________
Source: Mannsville 1991.
C. Trends
Future demand for nitrobenzene is almost exclusively dependent on
demand for aniline. Overall U.S. long-term aniline demand, and
therefore nitrobenzene demand, will probably increase at about 3 to 4
percent per year (Mannsville 1991).
The USITC has not reported production statistics for nitrobenzene
since 1986. Nitrobenzene output is generally in the range of 1.4
times derivative aniline output. The USITC (1994) reported the
production of aniline to be 1005 million pounds for 1992. There is
adequate capacity to meet domestic demand for nitrobenzene for several
years. Both Rubicon and First Chemical have expanded their
nitrobenzene production capacities in recent years (Mannsville 1991).
III. ENVIRONMENTAL FATE
A. Environmental Release
Depending on its purity, nitrobenzene is a pale yellow to yellow-brown,
oily liquid at room temperature. It has a characteristic
odor that has been associated with bitter almonds and shoe polish
(vapor pressure, 0.27 mm Hg @ 25øC) (U.S. EPA 1985; Budavari
1989). It is released into the environment primarily from
industrial uses but can also be formed in the atmosphere by the
nitration of benzene, a common air pollutant (ATSDR 1990). The
largest sources of nitrobenzene release are from its manufacture
and primary use as a chemical intermediate in the synthesis of
aniline (U.S. EPA 1985). The amounts of nitrobenzene released to
surface water and to land by industry have been greatly reduced
since 1988 (TRI92 1994). Smaller amounts are also released from
consumer products in which nitrobenzene is used as a solvent.
The most familiar of these are metal and shoe polishes (ATSDR
1990).
Nitrobenzene levels in air have been measured in urban, rural,
and waste disposal areas in New Jersey. Most air samples taken
in 1982 were negative for nitrobenzene, and the positive samples
taken from residential areas were about 0.3 parts per billion
(ppb) or less. Samples from industrial areas were 0.9 ppb or
more with the highest samples being 3.5 to 5.7 ppb. The
atmospheric nitrobenzene concentration was higher in the summer
than winter and lower during periods of heavy rain or snow. Air
samples taken over landfills in 1985, contained a maximum of
14.48 ppb nitrobenzene. Nitrobenzene has been detected in
samples taken during rain or snow (ATSDR 1990). In surface
water, nitrobenzene was detected in only 0.4% of 836 ambient
surface water stations, and in 1.8% of 1245 reporting stations on
industrial waste waters (ATSDR 1990). Soil samples taken along
the banks of the Buffalo River in New York contained 8 ppm
nitrobenzene in 1980, but the chemical was not found in sediment
samples (ATSDR 1990).
In 1992, releases of nitrobenzene to environmental media, as
reported to the Toxic Chemical Release Inventory by certain types
of U.S. industries, totaled about 917 thousand pounds. Of this
amount, 52 thousand pounds (5.6%) were released to the
atmosphere; 442 pounds (0.05%) were released to surface water;
and 865 thousand pounds (94.32%) were released in underground
injection sites; no nitrobenzene was reported to have been
released to land (TRI92 1994).
B. Transport
Nitrobenzene will volatilize slowly from soil and surface water
(vapor pressure, 0.27 mm Hg @ 25øC) and is subject to
biodegradation (U.S. EPA 1985). Adsorption to sediment and
bioconcentration are not thought to be significant fate processes
in water. Nitrobenzene may leach through the soil and is
considered to have intermediate mobility (ATSDR 1990).
C. Transformation/Persistence
1. Air Nitrobenzene apparently undergoes direct photolysis in
the atmosphere. Photoproducts formed from nitrobenzene in
the atmosphere include ortho- and para-nitrophenols, and
nitrosobenzene. Phenol was found as a photodegradation
product of nitrobenzene in the absence of oxygen (U.S. EPA
1985; ATSDR 1990). In laboratory tests, 38% of nitrobenzene
in air was photochemically degraded in 5 hours by
irradiation from a xenon lamp (U.S. EPA 1985; Howard 1989).
The chemical reacts slowly with hydroxyl radicals and ozone.
The half-lives calculated for reactions of nitrobenzene with
hydroxyl radicals and ozone in moderately polluted air are
90 days and 2 years, respectively (ATSDR 1990). Removal of
nitrobenzene from the atmosphere by wet deposition is not
believed to be significant (U.S. EPA 1985).
2. Soil Nitrobenzene is subject to biodegradation in the
soil, but the rates of decomposition based on screening
tests are conflicting. Results range from 98% removal in 5
days with activated sludge inoculum, to no degradation in 10
days with activated sludge inoculum. Higher concentrations
of nitrobenzene have been shown to be toxic to
microorganisms, but this explanation alone cannot account
for the varying results (Howard 1989; ATSDR 1990).
3. Water Nitrobenzene in solution is subject to
biodegradation and photodegradation; small amounts also
adsorb to sediment or volatilize from the surface. The
half-life of nitrobenzene in model waste stabilization ponds
was measured at 3.8 days; 89.5% of the added chemical was
degraded, 4.9% volatilized, 2.3% adsorbed to sediment, 2.3%
was lost in effluent, and 1% remained (Howard 1989). The
half-life of nitrobenzene in aquatic environments has been
estimated at 0.3 days by the U.S. EPA (1987).
4. Biota The bioconcentration factors in two species of fish,
L. idus (golden orfe) and P. promelas (fathead minnow), have
been estimated at 15 and less than 10, respectively (U.S.
EPA 1987). A bioconcentration factor of 3 has also been
calculated for P. reticulata (guppy) (Howard 1989).
Nitrobenzene is not expected to accumulate significantly in
aquatic organisms, however, it has been shown to be taken up
and may bioconcentrate in terrestrial plants (ATSDR 1990).
IV. HUMAN HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption Studies in humans and animals have demonstrated
that nitrobenzene is absorbed through the skin, the lungs,
and the gastrointestinal tract. The maximum dermal
absorption of liquid nitrobenzene was 0.2 - 3.0 mg/cm2/hour
(U.S. EPA 1985). When volunteers were exposed to 1 or 5.5
ppm nitrobenzene in air, it was estimated that about half of
the absorbed dose of nitrobenzene was absorbed through the
skin (ATSDR 1990). Volunteers breathing 6 ppm nitrobenzene
had an average absorption rate of 80% (ATSDR 1990; U.S. EPA
1985). Animal experiments have shown that nitrobenzene is
metabolized and excreted following oral administration.
Absorption from the gastrointestinal tract can also be
inferred from animal and human studies that demonstrate
toxic effects following the ingestion of nitrobenzene (U.S.
EPA 1985).
2. Distribution Two days after oral administration of 14[C]-
nitrobenzene to rabbits, about 56% of the radioactivity was
bound by the tissues, localized primarily in fat and the
intestinal tract. After 8 days, about 8% of the original
dose remained in the fat tissues. Analysis of the tissue
indicated that the radioactivity represented metabolites of
nitrobenzene rather than unaltered nitrobenzene (U.S. EPA
1985). The day after the oral administration of
radiolabeled nitrobenzene to rats the amount of
radioactivity bound to various tissues included 229 mmol/mol
bound to hemoglobin in the blood, 129 mmol/kg bound in
liver, 204 mmol/kg bound in kidney, and 62 mmol/kg bound in
lung (ATSDR 1990).
3. Metabolism The primary metabolite of nitrobenzene in
rabbits was reported to be p-aminophenol (U.S. EPA 1985).
This urinary metabolite accounted for 31-56% of the
administered oral dose within 2-5 days. Other metabolites
representing 3-9% of the oral dose included m-aminophenol,
o-aminophenol, p-nitrophenol, and m-nitrophenol. Minor
metabolites accounting for less than 1% of the administered
dose were identified as aniline, o-nitrophenol, 4-nitrocatechol,
nitroquinol, and p-nitrophenylmercapturic
acid (U.S. EPA 1985). p-Aminophenol was a major urinary
metabolite in mice, but did not appear in the urine of
either CD or Fischer 344 rats following oral exposure to
nitrobenzene. U.S. EPA (1995) has suggested this species
difference in nitrobenzene metabolism be considered when
discussing possible metabolism of nitrobenzene in humans.
Other urinary metabolites identified in rat and mouse
studies include p-hydroxyacetanilide, p-aminophenol,
p-nitrophenol, and m-nitrophenol. These metabolites have been
found in the free state and conjugated with glucuronide and
sulfate with varying frequencies in rats and different
strains of mice (U.S. EPA 1985). The reduction of
nitrobenzene by microflora of the intestinal tract appears
to occur following oral exposure. Sterilization of the
intestinal tract altered the proportion of urinary
metabolites excreted by rats, decreasing the excretion of
p-hydroxyacetanilide and an unidentified metabolite by 94 and
86%, respectively (U.S. EPA 1985).
4. Excretion Nitrobenzene metabolites are excreted in the
urine predominantly with smaller amounts excreted in feces
and in expired air. p-Nitrophenol and
p-aminophenol and their glucuronate and/or sulfate
conjugates have been identified in the urine of humans and
mice; p-aminophenol was apparently not excreted by the rat
strains tested. Rats eliminated a total of 75-79% of the
initial dose in 72 hours following oral administration of
14[C]nitrobenzene; 60.8-65.8% of the dose was found in the
urine. Mice were able to eliminate 54.3% of the
administered dose in 72 hours with 34.7% found in the urine.
The rest of the radioactivity recovered was found in the
feces (11.8-21.4%) and in expired air (0.8-2.5%) from the
rats and mice tested (U.S. EPA 1985). The major urinary
metabolites in humans are p-nitrophenol and p-aminophenol;
however, the metabolites are excreted more slowly than in
rats, mice, or rabbits. Urinary p-nitrophenol, which can be
utilized to estimate the nitrobenzene exposure level,
reached peak levels about 4 days after exposure (U.S. EPA
1985).
B. Acute Toxicity
The primary toxic effect resulting from acute exposure to
nitrobenzene by inhalation, oral or dermal routes is
methemoglobinemia and accompanying anoxia and erythrocyte damage.
Nervous system effects may also be experienced, but may be
partially due to the anoxia from the methemoglobinemia (see
section IV.G.).
1. Humans Inhalation exposure to nitrobenzene concentrations
equal to or greater than 6 ppm in air (30.72 mg/m3; 4.4
mg/kg/day) was reported to result in nervous system effects
(see section IV.G.) and methemoglobin production (U.S. EPA
1985). Sulfhemoglobinemia has also been observed following
nitrobenzene poisoning (U.S. EPA 1985). Atmospheric
concentrations of nitrobenzene resulting in these effects
are well above the odor threshold of 1.9 ppm, which may help
limit human exposures (U.S. EPA 1985). Oral exposures to
nitrobenzene have been reported, although rare and poorly
documented. Methemoglobinemia is the primary acute effect
following nitrobenzene ingestion. The dose resulting in
methemoglobinemia was estimated in one case study at 4.3 to
11 g based on urinary p-nitrophenol levels. A latency
period of 30 minutes to 12 hours, varying inversely with the
dose, followed ingestion (ATSDR 1990). Nitrobenzene is
rapidly absorbed through the skin and is a contact irritant
(Keith and Walters 1985).
2. Animals Increased methemoglobin production has been
reported in mice, rats, rabbits, and dogs following acute
exposure to nitrobenzene. Mice appear to be the most
resistant to methemoglobinemia probably because of a higher
level of methemoglobin reductase activity. However,
germ-free or antibiotic-treated rats do not develop
methemoglobinemia, which demonstrates a likely role of
intestinal bacteria in methemoglobin production in the rat
(U.S. EPA 1985). Hepatic lesions were recorded following a
single oral dose of nitrobenzene in rats (amount not given
in the secondary source) (U.S. EPA 1985).
LD50 values for various routes of administration have been
calculated for rats including 640 mg/kg for oral
administration and 2100 mg/kg for dermal administration
(U.S. EPA 1985). An inhalation LC50 value of 556 ppm was
calculated for Crl:CD rats exposed for 4 hours. Clinical
observations reported during exposure included cyanosis,
weakness, chromodacryorrhea, slight reddish-brown nasal
discharge, slight corneal clouding, and lacrimation.
Following exposure, survivors exhibited tremors, tachypnea,
weight loss, diarrhea, and prostration. Some animals were
hyperactive and exhibited aggressive behavior (TSCATS 1994).
C. Subchronic/Chronic Effects
Limited evidence suggests that the liver may be a target organ in
humans following extended inhalation exposure to nitrobenzene.
Adverse effects on the liver and kidneys have been reported in
animal studies. A lowest-observed-adverse-effect level of 25
mg/m3 was identified in rats and mice based on hematologic,
adrenal, renal, and hepatic lesions. This value was converted to
an equivalent continuous oral dose for mice and utilized by the
U.S. EPA (1994) to derive an oral reference dose (RfD) of 0.0005
mg/kg/day for nitrobenzene exposure.
1. Humans An enlarged liver, jaundice, and a decreased liver
function test (bromosulfophthalein retention) were reported
in a case history of a woman occupationally exposed to
unspecified concentrations of nitrobenzene for 17 months.
The exposure concentration for 2 of the 17 months has been
qualitativiely described as "high" (U.S. EPA 1985). The
consumption of alcohol has been reported to result in an
acute crisis including coma in individuals previously
exposed chronically or subchronically to nitrobenzene. In
one case history, an acute crisis was precipitated by the
consumption of one beer 6 weeks after recovering from a
subchronic nitrobenzene poisoning episode; however, no
numerical data on nitrobenzene exposure were given (U.S. EPA
1987).
2. Animals Groups of 10 male and 10 female Fischer 344 rats,
Sprague-Dawley CD rats, and B6C3F1 mice were exposed by
inhalation to nitrobenzene concentrations of 0, 5, 16, or 50
ppm (0, 25, 81, or 252 mg/m3), 6 hours/day, 5 days/week for
90 days. Increased methemoglobin levels were seen in
Fischer rats at 25 mg/m3, in Sprague-Dawley rats at 81
mg/m3, and in mice at 252 mg/m3. Hemosiderosis was seen in
the spleens of both rats and mice, but was mild in mice and
also occurred in the control group. Increased hematopoiesis
and hemolytic anemia including reticulocytosis was observed
at 81 mg/m3 in Fischer rats and at 252 mg/m3 in Sprague-Dawley
rats. Very slight to minimum nephrosis was recorded
for both rat strains at 25 mg/m3. Increased kidney weights
were seen at 252 mg/m3. No kidney effects were recorded in
mice. Nitrobenzene treatment resulted in liver lesions in
both rats and mice. Hepatocellular hypertrophy and Kupffer
cell pigmentation were observed in Sprague-Dawley rats at 25
mg/m3. At 81 mg/m3, increased periportal basophilia and
enlarged nucleoli were seen in rats, and centrilobular
hepatocellular hyperplasia was recorded for mice. Increased
severity and incidence of vacuolization of the adrenal zona
reticularis in female mice were also observed at 25 mg/m3
(U.S. EPA 1985). The 25 mg/m3 concentration defined a
lowest-observed-adverse level (LOAEL) for rats and mice
based on hematologic, adrenal, renal, and hepatic lesions
(U.S. EPA 1994). This value in mice was converted to an
equivalent continuous oral dose of 4.6 mg/kg/day and was
utilized by the U.S. EPA (1994) to calculate a chronic oral
RfD of 0.0005 mg/kg/day for nitrobenzene.
Inhalation exposure to 35 ppm for 2 weeks resulted in
hepatocyte necrosis in male Sprague-Dawley rats (ATSDR
1990).
D. Carcinogenicity
Nitrobenzene causes in rats and mice in lifetime inhalation
studies. This has been used as a basis for a recommendation to
classify nitrobenzene as a B2, probable human carcinogen.
1. Humans - No information was found in the secondary sources
search on the carcinogenicity of nitrobenzene in humans.
2. Animals - A recent assessment of the carcinogenicity of
nitrobenzene has been completed by U.S. EPA (1995). The
assessment is based on a single 1983 Chemical Industry
Institute of Toxicology inhalation study of both sexes of
B6C3F, F344/N rats, and Sprague-Dawely (CD strain) rats.
Mice were exposed to 0, 5, 25, and 50 ppm; rats, to 0, 1, 5,
and 25 ppm. Exposures were for 6 hours per day, 5 days per
week, for 104 weeks. Nitrobenzene induced tumors in several
sites over different species, sexes, and doses. Significant
increases in tumors were observed in the alveolus and
bronchus, the thyroid, and the mammary gland of mice.
F344/N rats showed significant increases in tumors of the
liver, the thyroid, the kidney, and the endometrium.
Sprague-Dawley (CD) rats showed significant increases in
tumors of the liver.
E. Genotoxicity
Results of short term mutagenicity testing show nitrobenzene is
not genotoxic. Nitrobenzene was negative in the Ames assay with
Salmonella typhimurium strains TA92, TA94, TA98, TA100, TA1537,
and TA1538 with, or without metabolic activation (U.S. EPA 1987).
Intragastric treatment of mice with nitrobenzene did not result
in micronuclei or chromosome aberrations in bone marrow cells or
dominant lethal mutations. No increase in unscheduled DNA
synthesis in rat hepatocytes was seen 12 hours following gavage
treatment with 200 or 500 mg/kg nitrobenzene (U.S. EPA 1987).
F. Developmental/Reproductive Toxicity
Animal studies have shown that inhalation exposure to
nitrobenzene can cause adverse testicular effects resulting in
decreased fertility index.
1. Humans No information was found in the secondary sources
searched on the developmental/reproductive toxicity of
nitrobenzene to humans.
2. Animals A decrease in fertility indices was recorded
following inhalation exposure to 40 ppm nitrobenzene, 6
hours/day, 7 days/week for 12 weeks prior to and including
the mating period in a two-generation study in rats.
Exposure was continued with the females through day 19 of
gestation. Microscopic examination revealed atrophy of the
seminiferous tubules, spermatocyte degeneration, absence of
mature sperm in the epididymis, and decreased testicular and
epididymal weights in both F0 and F1 generations. The
fertility index increased five-fold during 9 weeks of
recovery following exposure to nitrobenzene. There was no
observed maternal toxicity, and no effects on survival or
lactation indices at any dose tested ( 0, 1, 10, or 40 ppm)
(U.S. EPA 1987). Inhalation exposure of B6C3F1 mice, and
Fischer 344 and Sprague-Dawley rats to nitrobenzene
concentrations of 0, 5, 16, or 50 ppm, 6 hours/day, 5
days/week for 90 days resulted in severe degeneration of the
spermatogenic epithelium with decreased testicular weight,
and an absence of mature sperm in the epididymis of both rat
strains. Only slight effects were observed at the lower
doses, and no testicular changes were seen in the mice (U.S.
EPA 1987).
Inhalation studies have shown no fetotoxic, embryotoxic, or
teratogenic effects at concentrations up to 40 ppm in rats
and 100 ppm in rabbits. Maternal toxicity did occur at
these levels, demonstrated by increased methemoglobin levels
and increased spleen and liver weights (ATSDR 1990; U.S. EPA
1987).
Treatment of Fischer 344 and Sprague-Dawley rats with a
single oral dose of 300 mg/kg nitrobenzene resulted in
necrotic primary and secondary spermatocytes, multinucleated
giant cells, and decreased numbers of spermatocytes in the
epididymis within 1-4 days after treatment. These effects
were not seen at 50-200 mg/kg (U.S. EPA 1985).
G. Neurotoxicity
Adverse central nervous system effects can occur in humans and
animals following nitrobenzene exposure. Many of these effects
may be secondary to the anoxia resulting from methemoglobinemia.
1. Humans Exposure to nitrobenzene for up to 17 months was
reported to cause headache, nausea, vertigo, confusion,
hyperalgesia, and paresthesia (U.S. EPA 1985; ATSDR 1990).
Acute nervous system effects include nausea, nystagmus,
convulsions, and coma. Exposure to concentrations greater
than 40 ppm has resulted in intoxication. Methemoglobinemia
has also been shown to occur, and the resulting anoxia may
partially account for the nervous system effects (U.S. EPA
1985).
2. Animals Bilateral cerebellar perivascular hemorrhage and
cell breakdown in the hindbrain (cerebellar peduncle) were
seen in B6C3F1 mice and Sprague-Dawley rats exposed to 125
ppm nitrobenzene for two weeks. Fischer rats given
nitrobenzene at the same exposure level and duration did not
develop any brain lesions (ATSDR 1990).
V. ENVIRONMENTAL EFFECTS
Available information indicates that nitrobenzene is moderately toxic
to aquatic life. Several reported 96-hour LC50 values are in the
range of >1 mg/L to 100 mg/L.
A. Toxicity to Aquatic Organisms
Ninety-six-Hour LC50 values for fish are: 42.6 mg/L for Lepomis
macrohirus (bluegill sunfish), 117 mg/L for Pimephales promelas
(fathead minnow), 112.5 mg/L for Brachydanio rerio (zebrafish),
and 58.6 for Cyprinodon variegatus (sheepshead minnow). Forty-
eight-Hour LC50 values for fish are: 105 mg/L for Lepomis
macrohirus (bluegill sunfish), 156 mg/L for Pimephales promelas
(fathead minnow), 60-89 mg/L for Leuciscus idus melanotus (golden
orfe), 20 mg/L for Oryzias latipes (medaka), and >120 mg/L for
Cyprinodon variegatus (sheepshead minnow) (U.S. EPA 1985).
B. Toxicity to Terrestrial Organisms
Nitrobenzene is unlikely to exist in U.S. terrestrial
environments in sufficient concentrations to cause serious acute
or chronic effects to terrestrial organisms. Toxicity
information reported for rats, mice, and rabbits (see sections
IV.B.2., IV.C.2. and IV.G.) suggest that no acute effects would
be seen at normally expected U.S. environmental concentrations.
C. Abiotic Effects
Nitrobenzene reacts with hydroxyl radicals and ozone in the
atmosphere. In moderately polluted conditions the half-life of
nitrobenzene in the atmosphere may be reduced by a factor of 10.
The rate constant calculated for the reaction with ozone (5x1023
cm3/molecule-sec) indicates that the reaction has no
environmental significance (U.S. EPA 1985).
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list nitrobenzene as a hazardous
air pollutant. Occupational exposure to nitrobenzene is regulated by
the Occupational Safety and Health Administration (OSHA). The OSHA
permissible exposure limit (PEL) is 1 part per million parts of air
(ppm) as an 8-hour time-weighted average (TWA) (29 CFR 1910.1000). In
addition to OSHA, other federal agencies and groups may develop
recommendations to assist in controlling workplace exposure. These
agencies and groups (listed in Tables 4 and 5) should be contacted
regarding workplace exposures, and for additional information on
nitrobenzene.
TABLE 4. EPA OFFICES AND CONTACT NUMBERS INFORMATION ON
NITROBENZENE
________________________________________________________________________
EPA Office Statute Contact Number
________________________________________________________________________
Pollution Prevention EPCRA (313/TRI)a (800) 424-9346
& Toxics TSCA (8A, 8D, 4)b (800) 554-1404
Air Clean Air Act (919) 541-0888
(111, 112B)c
Solid Waste & RCRA (Action levels: (800) 424-9346
Emergency Response 2.0 æg/m3, air
0.02 mg/L, water
40 mg/kg, soil)d
CERCLA (RQ, 1000 pounds)e(800) 424-9346
SARA (110, 302A, 313)
Water Clean Water Act (304b, (202) 260-7588
307a, 311, CWA Priority)
WQC (17 æg/L [ao/do];
1900 æg/L [ao])f
_________________________________________________________________________
aEPCRA: Emergency Planning and Community Right to Know Act of 1986
bTSCA: Toxic Substances Control Act
cListed as hazardous air pollutant under 112 of Clean Air Act [42 U.S.C.
7401 et seq.]
dRCRA: Resource Conservation and Recovery Act (40 CFR 264.94). Action
Level: Health and environmental-based levels used by the EPA as indicators
for the protection of human health and the environment and as triggers for
a Corrective Measure Study.
eCERCLA: Comprehensive Environmental Response, Compensation, and Liability
Act of 1980, as amended. RQ: level of hazardous substance, which, if
equaled or exceeded in a spill or release, necessitates the immediate
reporting of that release to the National Response Center (40 CFR Part
302).
fWQC: Federal ambient water quality criteria for the protection of human
health (56 FR 58420). Ambient Water Quality Criteria standards:
established pursuant to the Clean Water Act, 57 FR 60848, December 22,
1992. ao/dw: protection for consuming aquatic organisms and drinking water;
ao: protection for consuming aquatic organisms.
TABLE 5. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON
NITROBENZENE
__________________________________________________________________________
Other Agency/Department/Group Contact Number
__________________________________________________________________________
Agency of Toxic Substances & Disease Registry (404) 639-6000
American Conference of Governmental
Industrial Hygienists (513) 742-2020
[TLV-TWA, 1 ppm (5 mg/m3),*]a
Consumer Product Safety Commission (301) 504-0994
Food & Drug Administration (301) 443-3170
National Institute for Occupational Safety & Health (800) 356-4674
[TWA, 1 ppm (5 mg/m3); IDLH, 200 ppm; *]b
Occupational Safety & Health Administration (202) 639-7960
[TWA, 1 ppm (5 mg/m3 ]c
_________________________________________________________________________
aTLV-TWA: Time-weighted-average concentration for a normal 8-hour workday
and a 40-hour workweek to which nearly all workers may be repeatedly
exposed without adverse effects; *: Skin designation, air sampling alone is
insufficient to accurately quantitate exposure. Measures to prevent
significant cutaneous absorption may be required (ACGIH 1994-1995).
bTWA: Time-weighted-average concentrations for up to a 10-hour workday
during a 40-hour workweek; IDLH: immediately dangerous to life or health
concentration, the maximum concentration from which, in the event of
respirator failure, one could escape within 30 minutes without a respirator
and without experiencing any escape-impairing or irreversible health
effects; *: Skin designation, air sampling alone is insufficient to
accurately quantitate exposure. Measures to prevent significant cutaneous
absorption may be required (NIOSH 1990; 1992).
cTWA: Time-weighted-average that must not be exceeded during any 8-hour
work shift of a 40-hour workweek.
Standard promulgated pursuant to the Occupational Safety and Health Act,
29 CFR 1910 (OSHA 1993).VII. CITED REFERENCES
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